THC Stats - Substance Search

Pharmacology

DrugBank

State Solid

Description

Dronabinol (marketed as Marinol) is a synthetic form of delta-9-tetrahydrocannabinol (Δ⁹-THC), the primary psychoactive component of cannabis (marijuana). THC demonstrates its effects through weak partial agonist activity at Cannabinoid-1 (CB1R) and Cannabinoid-2 (CB2R) receptors, which results in the well-known effects of smoking cannabis such as increased appetite, reduced pain, and changes in emotional and cognitive processes. Due to its evidence as an appetite stimulant and an anti-nauseant, Dronabinol is approved for use in anorexia associated with weight loss in patients with AIDS and for the treatment of nausea and vomiting associated with cancer chemotherapy in patients who have failed to respond adequately to conventional antiemetic treatments . Tetrahydrocannabinol (THC) and cannabidiol (CBD) are the two most abundant cannabinoids found naturally in the resin of the marijuana plant, both of which are pharmacologically active due to their interaction with cannabinoid receptors that are found throughout the body . While both CBD and THC are used for medicinal purposes, they have different receptor activity, function, and physiological effects. If not provided in their activated form (such as through synthetic forms like Dronabinol or DB00486), THC and CBD are obtained through conversion from their precursors, tetrahydrocannabinolic acid-A (THCA-A) and cannabidiolic acid (CBDA), through decarboxylation reactions.

Mechanism of Action

Dronabinol is a synthetic form of delta-9-tetrahydrocannabinol (Δ⁹-THC), the primary psychoactive component of cannabis (marijuana). THC demonstrates its effects through weak partial agonist activity at Cannabinoid-1 (CB1R) and Cannabinoid-2 (CB2R) receptors, which results in the well-known effects of smoking cannabis such as increased appetite, reduced pain, and changes in emotional and cognitive processes.

Pharmacodynamics

Marinol may has complex effects on the central nervous system (CNS), including cannabinoid receptors. Dronabinol may inhibit endorphins in the emetic center, suppress prostaglandin synthesis, and/or inhibit medullary activity through an unspecified cortical action.

Metabolism

THC is primarily metabolized in the liver by microsomal hydroxylation and oxidation reactions catalyzed by Cytochrome P450 enzymes. 11-hydroxy-▵9-tetrahydrocannabinol (11-OH-THC) is the primary active metabolite, capable of producing psychological and behavioural effects, which is then metabolized into 11-nor-9-carboxy-▵ 9-tetrahydrocannabinol (THC-COOH), THC's primary inactive metabolite . Dronabinol and its principal active metabolite, 11-OH-delta-9-THC, are present in approximately equal concentrations in plasma. Concentrations of both parent drug and metabolite peak at approximately 0.5 to 4 hours after oral dosing and decline over several days .

Absorption

Dronabinol capsules are almost completely absorbed (90 to 95%) after single oral doses. Due to the combined effects of first pass hepatic metabolism and high lipid solubility, only 10 to 20% of the administered dose reaches the systemic circulation. After oral administration, dronabinol has an onset of action of approximately 0.5 to 1 hours and peak effect at 2 to 4 hours. Following BID dosing of 2.5mg of dronabinol, Cmax was found to be 1.32ng/mL with a median Tmax of 1.00 hr.

Indication

For the treatment of anorexia associated with weight loss in patients with AIDS, and nausea and vomiting associated with cancer chemotherapy in patients who have failed to respond adequately to conventional antiemetic treatments

Half-life

The elimination phase of dronabinol can be described using a two compartment model with an initial (alpha) half-life of about 4 hours and a terminal (beta) half-life of 25 to 36 hours.

Protein Binding

The plasma protein binding of dronabinol and its metabolites is approximately 97%.

Elimination

Dronabinol and its biotransformation products are excreted in both feces and urine. Because of its large volume of distribution, dronabinol and its metabolites may be excreted at low levels for prolonged periods of time. Following single dose administration, low levels of dronabinol metabolites have been detected for more than 5 weeks in the urine and feces.

Volume of Distribution

Dronabinol has a large apparent volume of distribution, approximately 10 L/kg, because of its lipid solubility.

Clearance

Values for clearance average about 0.2 L/kg-hr, but are highly variable due to the complexity of cannabinoid distribution.

Measured Affinities

Guide to PHARMACOLOGY

Measured binding and functional data for Δ9-tetrahydrocannabinol, curated by the IUPHAR/BPS Guide to PHARMACOLOGY. Each row cites the paper it came from. Lower concentrations mean tighter binding — a value in the sub-nanomolar range indicates a very potent interaction.

Target	Action	Measure	Value	Concentration	Species	Source
GPR55 GPR55	Agonist	pEC50	8.1	7.94 nM	Human	PMID 17876302
GPR18 GPR18	Full agonist	pEC50	6.02	954.99 nM	Human	—
glycine receptor α2 subunit GLRA2	Potentiation	pEC50	6	1,000 nM	Human	—
glycine receptor α1 subunit GLRA1	Potentiation	pEC50	5.5	3,162 nM	Human	—
glycine receptor α3 subunit GLRA3	Potentiation	pEC50	5.3	5,012 nM	Human	—
TRPA1 TRPA1	Agonist	pEC50	4.9	12,589 nM	Human	PMID 14712238
TRPV2 Trpv2	Activation	pEC50	4.85	14,125 nM	Rat	PMID 18550765
CB1 receptor CNR1	Partial agonist	pKi	—	—	Human	—
CB2 receptor CNR2	Partial agonist	pKi	—	—	Human	—

Reading this. pKi, pEC50 and pIC50 are negative log molar values, so a higher number means a tighter interaction; the concentration column converts them for you. Values from non-human species are laboratory measurements and do not translate directly to human effect. Receptor affinity is not a dose — it describes what a molecule binds, not how much of it is safe to take.

Receptor data from the IUPHAR/BPS Guide to PHARMACOLOGY (v2026.2), licensed CC BY-SA 4.0. Matched to this substance by InChIKey.

Toxicity

PsychonautWiki PubChem

Despite its reputation for being a benign substance, it is important to be aware that cannabis use is associated with distinct risks. Acute adverse effects include anxiety, hyperemesis syndrome, impaired coordination and judgment, suicidal ideations/tendencies, and psychotic symptoms.

Carcinogenicity

Under the conditions of these 2-year gavage studies, there was no evidence of carcinogenic activity of 1-trans-delta9-tetrahydrocannabinol in male or female F344/N rats administered 12.5, 25, or 50 mg/kg. There was equivocal evidence of carcinogenic activity of THC in male and female B6C3F1 mice based on the increased incidences of thyroid gland follicular cell adenomas in 125 mg/kg groups.

Liver injury risk

Ambiguous (limited data)

FDA LiverTox / DILIrank. Reflects published case reports of liver injury, not absolute risk.

Addiction & dependence

Cannabis is moderately habit-forming. Research has shown the overall dependence potential for cannabis to be less than that for caffeine, tobacco, alcohol, cocaine or heroin, but higher than that for psilocybin, mescaline, or LSD. Dependence on cannabis is more common amongst heavy users.

Tolerance & Pharmacokinetics

drugs.wiki

Half-Life

≈ 1–3 days (occasional users), prolonged up to ~13 days with chronic use due to adipose redistribution

Addiction Potential

Low–moderate. Psychological dependence possible; physical dependence mild. Withdrawal typically irritability, sleep disturbance, decreased appetite.

Tolerance Decay

Full tolerance 10d Half tolerance 14d Baseline ~28d

Based on human imaging and clinical studies showing CB1 down‑regulation with daily use and reversal over days–weeks. Model is approximate and varies with dose, frequency, and route. Data quality: mixed clinical/anecdotal.

Cross-Tolerances

Other CB1‑active cannabinoids

Experience Report Analysis

Erowid

4,950 Reports

1,313 Single-substance

1991–2025 Date Range

1,791 With Age Data

30 Effects Detected

Demographics

Gender Distribution

Age Distribution

Reports Over Time

Effect Analysis

Erowid

Effects aggregated from 1,313 experience reports (1,313 single-substance Erowid)

1,313 Reports

30 Effects Detected

11 Positive

11 Adverse

8 Neutral

Effect Sentiment Distribution

Confidence Distribution

Each bar is the share of reports mentioning the effect; its whisker, and the band on the rows below, is the 95% interval: where the share could plausibly be with other reports of the same kind.

Positive Effects 11

Music Enhancement 28.8% 70%

Color Enhancement 23.5% 70%

Empathy 22.2% 70%

Euphoria 19.6% 70%

Stimulation 18.5% 70%

Sedation 14.9% 70%

Introspection 10.2% 70%

Tactile Enhancement 9.5% 70%

Body High 9.4% 70%

Focus Enhancement 9.2% 70%

Creativity Enhancement 3.2% 70%

Adverse Effects 11

Anxiety 58.1% 70%

Confusion 29.0% 70%

Nausea 12.6% 70%

Memory Suppression 12.4% 70%

Increased Heart Rate 7.8% 70%

Motor Impairment 6.9% 70%

⚠ Psychosis 4.5% 70%

Headache 4.3% 70%

Muscle Tension 2.8% 70%

Sweating 2.7% 70%

⚠ Seizure 2.5% 70%

Show 8 neutral or unclassified mentions

Visual Distortions 25.5%

Auditory Effects 21.6%

Dissociation 18.1%

Closed-Eye Visuals 16.2%

Hospital 11.0%

Open-Eye Visuals 6.8%

Time Distortion 6.2%

Ego Dissolution 2.4%

Also reported in combinations. In the 3,637 THC reports where another drug was taken too, 362 (10.0%) mention hospital, emergency services or an overdose, 87 (2.4%) a seizure and 151 (4.2%) psychosis. In the 1,313 single-substance reports: 11.0%, 2.5% and 4.5%. These are not in the figures above: they cannot be put down to THC alone, and a mention is not always something that happened to the writer.

Dosage Distribution

Dose distribution from experience reports, one dose per report (the first listed). Doses above Q3 + 3×IQR, far above what people typically take, are left out of the median and range and listed under each route: most are real heavy doses or overdoses, not mistakes.

Smoked (cannabis, by weight)

Weight of cannabis as reported (flower, hash, edibles or extracts), not of THC, so it cannot be read against the THC dose ladder.

Median: 1.0 g IQR: 0.5–1.5 g n=233

7 reports gave a dose above the typical range (5–10 g), so they are not in the figures above. Listing a dose here does not mean it is safe.

Show the reports

10 g
7 g · another drug taken too
7 g · another drug taken too
6 g · another drug taken too
5 g · another drug taken too
5 g · another drug taken too
5 g · another drug taken too

Oral (cannabis, by weight)

Weight of cannabis as reported (flower, hash, edibles or extracts), not of THC, so it cannot be read against the THC dose ladder.

Median: 1.5 g IQR: 0.77–4.5 g n=57

1 report gave a dose above the typical range (23 g), so it is not in the figures above. Listing a dose here does not mean it is safe.

Show the report

23 g

Oral

Median: 10.0 mg IQR: 6.2–15.0 mg n=10

1 report gave a dose above the typical range (80 mg), so it is not in the figures above. Listing a dose here does not mean it is safe.

Show the report

80 mg

Real-World Dose Distribution

Erowid

From 24 of 28 recorded dose entries: those that state a weight (mg, g or µg), in routes with at least five of them. Values above Q3 + 3×IQR, far above what people typically take, are left out; they can include real heavy doses and overdoses, not only mistakes.

Oral (n=23)

Median: 10.0mg 25th: 5.0mg 75th: 10.0mg 90th: 19.0mg

Common Combinations

Most co-occurring substances, as a share of all 4,950 reports filed under THC; whiskers are 95% intervals

Form / Preparation

Most common forms and preparations, as a share of the 2,755 reports that give one; whiskers are 95% intervals

Body-Weight Dosing

Dose per kg of body weight, one dose per report (the first listed), from reports giving a weight of 30–250 kg. Doses above Q3 + 3×IQR, far above what people typically take, are left out of the median and range and listed under each route.

Median: 0.153 mg/kg IQR: 0.086–0.215 mg/kg n=10

1 report gave a dose above the typical range (0.735 mg/kg), so it is not in the figures above. Listing a dose here does not mean it is safe.

Show the report

0.735 mg/kg

Redose Patterns

Redosing behavior across 3695 reports

13.2% Redosed

1.2 Avg Doses

120m Median Interval

Harm Reduction

drugs.wiki

Harm‑reduction additions and clarifications:

• “Start low, go slow,” especially with edibles: Oral THC has low/variable bioavailability and first‑pass conversion to 11‑hydroxy‑THC, which is more psychoactive and longer‑acting. Wait at least 2 hours before considering redosing to avoid delayed over‑intoxication. High‑fat meals can significantly increase oral THC exposure.

• Driving: Simulator and epidemiologic data indicate meaningful impairment for several hours after use, often beyond users’ self‑perception. Avoid driving or operating hazardous machinery for a minimum of 4–6 hours after inhalation and longer after higher oral doses; co‑use with alcohol markedly magnifies crash risk. THC can remain detectable long after impairment has resolved, especially in frequent users.

• Inhaled vapes: Avoid illicit/counterfeit THC cartridges; vitamin E acetate and other diluents were strongly linked to EVALI cases in 2019. Prefer regulated, tested products if vaping at all.

• Cannabinoid Hyperemesis Syndrome (CHS): Chronic, heavy use can cause cyclic vomiting relieved by hot showers; topical capsaicin may help acutely, but complete cessation is the definitive treatment.

• Cardiovascular and orthostatic effects: THC can cause tachycardia and vasodilation with orthostatic hypotension; people with significant cardiovascular disease should avoid or minimize THC.

• Mental health: Higher‑THC exposure, early onset, and heavy/frequent use are associated with increased risk of anxiety symptoms and psychotic‑like experiences; avoid if you have a personal or strong family history of psychosis, and prefer lower‑THC/higher‑CBD products if using.

• Adolescents/young adults: Because brains are still developing, initiate use later if at all; frequent adolescent use is linked to worse mental‑health and cognitive outcomes.

• Pregnancy and lactation: Avoid cannabis/CBD during pregnancy and while breastfeeding. THC crosses the placenta and is excreted into breast milk for days to weeks; potential neurodevelopmental risks are uncertain but concerning.

• Storage and pediatric safety: Edibles are a common source of accidental pediatric intoxication; store products in child‑resistant containers, locked and out of sight.

• Product variability: Non‑prescription CBD products and some cannabis edibles can be mislabeled for potency and purity; use lab‑tested, regulated sources when possible.

• Tolerance: With frequent use, CB1 down‑regulation produces tolerance to many subjective effects; tolerance reverses over days to weeks of abstinence, which also reduces withdrawal symptoms (sleep disturbance, irritability, appetite change).

• Genetics/phenoconversion: CYP2C9 poor metabolizers, or those taking CYP2C9 inhibitors, may experience stronger/longer effects from oral THC; start with lower doses.

THC Stats & Data

Pharmacology

Description

Mechanism of Action

Pharmacodynamics

Metabolism

Absorption

Indication

Half-life

Protein Binding

Elimination

Volume of Distribution

Clearance

Measured Affinities

Toxicity

Carcinogenicity

Liver injury risk

Addiction & dependence

Tolerance & Pharmacokinetics

Tolerance Decay

Cross-Tolerances

Experience Report Analysis

Demographics

Gender Distribution

Age Distribution

Reports Over Time

Effect Analysis

Effect Sentiment Distribution

Confidence Distribution

Positive Effects 11

Adverse Effects 11

Dosage Distribution

Smoked (cannabis, by weight)

Oral (cannabis, by weight)

Oral

Real-World Dose Distribution

Oral (n=23)

Common Combinations

Form / Preparation

Body-Weight Dosing

Redose Patterns

Harm Reduction

References

Cited references